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Genetic risks of antiviral nucleoside analogues--a survey

P Wutzler1, R Thust

  • 1Institute for Antiviral Chemotherapy, Friedrich Schiller University of Jena, Winzerlaer Str. 10, 07745, Jena, Germany.

Antiviral Research
|March 15, 2001
PubMed

Insights

Most antiviral nucleoside analogues cause genetic damage in cells but are not mutagenic. While some drugs like zidovudine (AZT) show carcinogenicity in rodents, human data is inconclusive, supporting their therapeutic use.

Area of Science:

  • Pharmacology
  • Toxicology
  • Genetics

Background:

  • Nucleoside analogues are widely used as antiviral agents.
  • Concerns exist regarding their potential genotoxic and carcinogenic effects.

Purpose of the Study:

  • To review genotoxic and carcinogenic data for common antiherpesvirus and antiretroviral nucleoside analogues.
  • To assess the relevance of experimental findings to human risk.

Main Methods:

  • Compilation and review of published data on genotoxicity (chromosomal aberrations, gene mutations) and carcinogenicity in experimental systems.
  • Analysis of findings for aciclovir, penciclovir, ganciclovir, brivudine, cidofovir, zidovudine (AZT), lamivudine, zalcitabine (ddC), didanosine, and stavudine.

Main Results:

  • Most nucleoside analogues induced chromosomal aberrations in experimental systems.
  • These drugs were generally inactive in gene mutation assays.
  • Carcinogenicity findings in rodents were variable, with clear positive results for zidovudine (AZT) and zalcitabine (ddC).
  • Mechanisms of genetic damage remain largely hypothetical.
  • Experimental data could not be directly extrapolated to human risk.
  • No conclusive evidence linked these drugs to human tumors.

Conclusions:

  • Nucleoside analogues can induce genotoxic effects like chromosomal aberrations.
  • Carcinogenicity in humans has not been conclusively demonstrated.
  • The use of nucleoside analogues in antiviral therapy is supported by a favorable risk/benefit assessment.

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